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1 Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama, United States; Geriatric Research, Education, and Clinical Center, VA Medical Center, Birmingham, Alabama, United States
2 Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama, United States; Geriatric Research, Education, and Clinical Center, VA Medical Center, Birmingham, Alabama, United States; Medical Scientist Training Program, University of Alabama at Birmingham, Birmingham, Alabama, United States
3 Surgery, University of Alabama at Birmingham, Birmingham, Alabama, United States
* To whom correspondence should be addressed. E-mail: mbamman{at}uab.edu.
We applied K-means cluster analysis to test the hypothesis that muscle-specific factors known to modulate protein synthesis and satellite cell activity would be differentially expressed during progressive resistance training (PRT, 16 wk) in 66 human subjects experiencing extreme, modest, and failed myofiber hypertrophy. Muscle mRNA expression of IGF-IEa, mechanogrowth factor (MGF, IGF-IEc), myogenin, and MyoD were assessed in muscle biopsies collected at baseline (T1) and 24 h after the first (T2) and last (T3) loading bouts from previously untrained subjects clustered as extreme (XTR, n=17), modest (MOD, n=32), and non-responders (NON, n=17) based on mean myofiber hypertrophy. Myofiber growth averaged 2475 µm2 in XTR, 1111 µm2 in MOD, and -16 µm2 in NON. Main training effects revealed increases in all transcripts (46-83%, P<0.005). For the entire cohort, IGF-IEa, MGF, and myogenin mRNAs were up-regulated by T2 (P<0.05) while MyoD did not increase significantly until T3 (P<0.001). Within clusters, MGF and myogenin up-regulation was robust in XTR (126% and 65%) and MOD (73% and 41%) vs. no changes in NON. While significant in all clusters by T3, IGF-IEa increased most in XTR (105%) and least in NON (44%). Although MyoD expression increased overall, no changes within clusters were detected. We reveal for the first time that MGF and myogenin transcripts are differentially expressed in subjects experiencing varying degrees of PRT-mediated myofiber hypertrophy. The data strongly suggest the load-mediated induction of these genes may initiate important actions necessary to promote myofiber growth during PRT, while the role of MyoD is less clear.
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